Ask about this productRelated genes to: FEN1 antibody
- Gene:
- FEN1 NIH gene
- Name:
- flap structure-specific endonuclease 1
- Previous symbol:
- RAD2
- Synonyms:
- FEN-1, MF1
- Chromosome:
- 11q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-02-03
- Date modifiied:
- 2016-10-05
Related products to: FEN1 antibody
Related articles to: FEN1 antibody
- Arsenic poisoning significantly elevates the risk of cancer and other chronic illnesses. The goal of this research is to identify important genes whose expression changes in response to arsenic toxicity, and the molecular pathways affected by arsenic, using computational analysis of arsenic toxicity profiles. This approach will computationally identify and analyze genes whose expression changes in response to arsenic, thereby elucidating the heightened risk of carcinogenesis in arsenic-exposed individuals. This work employed high-throughput arsenic toxicity profiles to computationally identify and analyze expressed genes (DEGs) differentially in Affymetrix microarray datasets from the Gene Expression Omnibus (GEO) database, which were screened using the GEO2R program. A protein-protein interaction (PPI) network was constructed using STRING to elucidate the functional links between these DEGs and DNA repair genes. Interactions between the seven central genes (E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS) and the repair genes PARP1, NBN, PMS1, MSH3, XRCC5, XRCC6, MGMT, and MLH1 were discovered. We employed the DAVID and Enrichr-KG platforms to investigate the functions of these genes and their associations with cellular and molecular processes in greater detail. Two hundred eighty-one non-synonymous single-nucleotide polymorphisms (nsSNPs) in the 07 genes linked to arsenic toxicity were found using the COSMIC database. Based on our analysis, mutations in E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS can hinder DNA repair mechanisms, ultimately leading to cancer. Our computational analysis demonstrated that these non-synonymous SNPs can affect gene function, potentially altering protein stability and activity. Furthermore, according to Metal-Protein docking and protein-protein docking, these genes and their mutations appear to affect interactions with repair proteins substantially. Specific dietary consumption may lessen the detrimental effects of arsenic poisoning on protein function. We hypothesized that the mutations might be reversed by attaching particular molecules to these mutants. The protective effects of six curcumin compounds were examined using molecular docking with AutoDock 4.2.6 to assess protein dynamics and binding interactions. Optimal complexes were selected for dynamics simulation using GROMACS, and potential strategies for long-term cancer prevention related to arsenic exposure were identified. - Source: PubMed
Parida LuckyPatel Trupti N - Okazaki fragment maturation (OFM), the process that removes RNA-DNA primers, is a major source of DNA replication stress and mutations. It involves PolĪ“-mediated DNA strand displacement synthesis that produces 5' flaps, FEN1-mediated 5' flap cleavage, and LIG1-catalyzed nick ligation. Recently, we discovered that under hyperthermal stress conditions, yeast cells convert 5' flaps into 3' flaps, which are degraded by 3' flap nucleases to produce DNA nicks. However, little is known about this 3' flap-based OFM in human cells. Here, we report that 3' flaps frequently form in various human cancer cells, and that FEN1 deficiency significantly enhances 3' flap levels. XPF1 is recruited to the replication forks in FEN1 mutant or FEN1-chemically inhibited cells. Notably, XPF deficiency or inhibition in those defective cells leads to accumulation of 3' flaps, replication-related DNA strand breaks, and unique mutation signatures. Furthermore, XPF and FEN1 inhibitors show synergistic effects in killing human cancer cells. In summary, we demonstrate that 3' flap-based OFM is an important alternative of 5' flap-based OFM in mammalian cells. XPF is a key nuclease to degrade 3' flaps and complete OFM for survival. Targeting this compensatory mechanism could provide new therapeutic strategies to selectively impair cancer cell survival under replication stress. - Source: PubMed
Li KejiaoYang FengWang YingyingShi GuojunWang YixingLiu YunhaoYan YaoLei YiZhou MainSun HaitaoZheng LiShen Binghui - Neuroblastoma (NB) is the most common extracranial solid tumor in children with poor overall survival. Increasing evidence indicates that telomeres contribute to tumorigenesis and influence cancer prognosis. However, the biological and clinical implications of telomere-related genes (TRGs) in NB remain poorly defined. - Source: PubMed
Publication date: 2026/05/18
Aierken YeerfanZheng LuluLiu TaoTan KezheLv Zhibao - Colorectal adenoma (CRA) is a precancerous lesion that can progress to colorectal carcinoma (CRC); however, its malignant potential varies considerably. The present study aimed to characterize the putatively pathogenic variants (PPVs) of CRA and to assess their potential clinical relevance in identifying lesions with an increased risk of progression at precancerous stages. PPVs in a panel of 176 cancer-associated genes were analyzed in 67 CRA samples and matched adjacent normal mucosa using next-generation sequencing. The panel included genes involved in DNA repair pathways, cell cycle regulation and the genes directly associated with CRC development. PPVs in CRA tissue were identified in 44 patients. The most frequently mutated genes were found to be and , with mutations being the most prevalent. A higher frequency of PPVs was observed in CRA with high-grade dysplasia and tubulo-villous features. Notably, among the entire sample set, there were 10 hyperplastic polyps, which are generally considered low risk; however, three carried PPVs, specifically one polyp carried and mutations, another polyp carried and mutation, and a third carried a mutation. These findings suggested that mutational profiling may provide additional molecular information beyond histopathological assessment and could support improved risk stratification of colorectal lesions in early, precancerous stages. Such molecular characterization may be of value for identifying subsets of patients who could benefit from closer clinical surveillance. - Source: PubMed
Publication date: 2026/05/04
Valickova AnnaUrbanova MarketaHorak JosefJungwirth JiriKral JanHucl TomasMakajevova VeronikaSummerova SandraKohout PavelMatej RadoslavVodicka PavelVymetalkova Veronika - Osteosarcoma (OS) is the most prevalent primary malignant bone tumor in children. We previously showed that rotenone suppressed OS cell metastasis. However, its effects on OS cell growth and the underlying mechanisms remain unclear. The purpose of this study was to investigate the role of rotenone in OS and identify its direct target. - Source: PubMed
Publication date: 2026/05/04
Li ZhenMa XiangMa HengweiChen BaoJiang KunZhu ZiqiangWang JianqiangWang BaoqingWang YunqingDong Suwei